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Introduction

Untreated, depression can result in disability and death.1 It is present in at least 17% of patients who present to GPs2 and has a 12-month prevalence of 5% and a lifetime risk of 15%.3 It is often unrecognised,1 yet moderate to severe depression is as disabling as congestive heart failure.1 Further, depression is the leading cause of disability for all conditions among both sexes, both in Australia and worldwide.4,5 The lifetime risk of suicide in patients diagnosed with depression is 6% and treatment halves this risk.1

Despite being treatable, 60% of sufferers have not used any form of health service in the previous months.4 Lack of awareness, stigma and shame on behalf of the patient contribute to this. Of those receiving treatment, three-quarters will be managed in general practice.5,6 As Whitford4 notes:

It is clear that the main focus of activity aimed at reducing the burden of common mental health disorders in Australia is in primary care. Specialist mental health services play a supporting, but not central, role.

Depression is a chronic relapsing organic brain disease. Its mean onset is at 27 years of age. However, 40% of sufferers present by 20 years of age.7 The average duration of episodes is 3–4 months and 40% of patients will relapse within a 12-month period.7

The cause of depression is multifactorial, having biological, psychological and social factors. Mood disorders in general have a strong familial tendency, and the risk of developing a depressive disorder can be thought of in terms of a ‘stress-vulnerability model’. That is, an individual may have a genetically determined vulnerability and if enough stress is endured a mood disorder may result. Those who are more genetically vulnerable require less stress, but if enough stress is applied, any individual can develop a mood disorder.

When stress is present, the more vulnerable individual will develop increased glucocorticoid activity. This leads to increased neuronal mitochondrial activity, which can result in ‘mitochondrial dropout’ and neuronal death.

Stress will also lead to a decrease in the protective brain-derived neurotrophin factor (BDNF), which can result in neuronal death—also referred to as ‘glional dropout’. Serotonin, noradrenalin and to a lesser extent dopamine lead to RNA replication of BDNF, and the complicated and poorly understood biochemical cascade that occurs ‘beyond the receptor’ is the reason for the slow response to antidepressants.

The result of this neuronal trauma leads to decreased activity in the prefrontal cortex and increased activity in the limbic system, particularly the amygdala and hippocampus. This traumatic effect on the brain of prolonged stress can actually ...